As a GLP-1 agonist, it mimics the physiological effects of naturally released GLP-1 in the body.
In response to glucose intake, PPG neurons in the central nervous system (CNS) and L-cells in the gut produce and secrete GLP-1, an inhibitory gastrointestinal hormone.
After being released, GLP-1 activates GLP-1R receptors on pancreatic β-cells, triggering a series of metabolic changes characterized by insulin secretion and appetite suppression.
Insulin secretion leads to an overall reduction in blood glucose levels, decreased glucagon production, and prevention of glucose release from the liver’s glycogen stores. This induces satiety, improves insulin sensitivity, and ultimately results in weight loss.
The drug stimulates insulin secretion in a glucose-dependent manner, thereby lowering the risk of hypoglycemia. In addition, it has positive long-term effects on the survival, proliferation, and regeneration of β-cells.
Research shows that semaglutide primarily mimics the effects of GLP-1 released from the gut rather than from the brain. This is because most GLP-1 receptors in the brain lie outside the effective range of these systemically administered drugs. Despite its limited direct action on brain GLP-1 receptors, semaglutide remains highly effective in reducing food intake and body weight.
It appears to achieve this by activating neuronal networks across the central nervous system, many of which are secondary targets that do not directly express GLP-1 receptors.
In 2024, approved commercial versions of semaglutide include Ozempic, Rybelsus, and Wegovy injections, all developed by Novo Nordisk.
Post time: Aug-18-2025